The skin is made up of two primary layers that differ in function, thickness, and strength. From outside to inside, they are the epidermis and its sub-layers, and the dermis, after which is found subcutaneous tissue, or the hypodermis.
The epidermis of the skin is a non-vascularized layer of the skin. Different factors can result in increased blood vessel formation in the papillary dermis and these blood vessels may sometimes extend into the epidermis resulting in clinically significant skin manifestations. For example, over-activated keratinocytes actively producing and secreting pro-angiogenic factors in the form of growth factors or cytokines can result in increased blood vessel formation in the papillary dermis, which may sometime extend into the epidermis. Epidermal microvascular proliferation ultimately leads to epidermal keratinocyte hyperproliferation, thickening of the epidermis with parakeratosis of the stratum corneum and inflammatory infiltrate around the blood vessels in the papillary dermis. The microvascular changes are also characterized by increased tortuosity of dermal capillary loops which precede the development of epidermal hyperplasia.
Histological studies, including immunocytochemistry, routine histology and electron microscopy have clearly established that alterations in the blood vessel formation of the skin discussed above are a prominent feature in chronic inflammatory skin conditions, including psoriasis, eczema, rheumatoid arthritis, burn granulations, and hypertrophic scars. In psoriasis, for example, there is a marked increase in the cutaneous blood active edge of the psoriatic plaque [Braverman I M, Yen A. Ultrastructure of the capillary loops in the dermal papillae of psoriasis. J Invest Dermatol 1977: 68: 53-60].
The regression of dermal vessel tortuosity and of spongiform pustules in patients suffering from chronic inflammatory skin conditions provides the patient with benefits including but not limited to: reduced inflammation, reduced inflammatory edema, reduced erythema, reduced pain, reduced itching, help in resolving lesions and assistance in changing the epidermis to its normal non-vascularized state.
The epidermis, the outermost layer of skin, is thin but complex. Melanin, which is responsible for skin pigmentation, is found throughout the epidermis. The epidermis also keratinizes to produce nails, hair, sweat, and to regenerate.
Keratinization, the maturation and migration of skin cells, begins in the innermost layer of the epidermis, the stratum germinativum. These cells, called keratinocytes, accumulate and move outward toward the next epidermis layer, the stratum spinosum, where they become dense. The next layer, known as the stratum granulosum layer, contains 1 to 3 rows of flattened cells whose cytoplasm contain small granules. The granules contain proteins being transformed into the waterproofing protein keratin. It is in this layer that one finds glycolipids and a thickening of the membrane. A protein called filigrin is made in this layer and is put in the granules. In this layer, cells lose their nuclei. In the cytoplasm, there are keratohyalin granules as well as membrane-coating granules which expel their lipid contents into the intercellular spaces. Lipids assist in the formation of water barriers among the cells of the skin, which, in turn, help to ensure body moisturization. At this point, the cell also becomes flattened, or horny, and the nucleus disappears; what remains is keratin. In the next layer, the stratum lucidum, the cell is prepared to move into its final sub-layer with the addition of melanin granules. Then, sudden changes in enzyme function cause cell death. The products of this ongoing process form the stratum corneum, which is the outermost epidural layer consisting of neatly packed dead horny cells.
Keratinization disorders in the stratum granulosum layer in the epidermis can often lead to clinically significant skin manifestations. One common disorder includes thinning of the stratum granulosum layer due to malfunctioning of the keratinization process leading to reduction in the moisture barrier properties of the stratum granulosum layer. In addition, for example, over activated keratinocytes actively producing and secreting pro-angiogenic factors in the form of growth factors or cytokines can result in increased blood vessel formation in the papillary dermis which may sometime extend into the epidermis. Epidermal microvascular proliferation ultimately leads to epidermal keratinocyte hyperproliferation, thickening of the epidermis with parakeratosis of the stratum corneum and inflammatory infiltrate around the blood vessels in the papillary dermis. The microvascular changes are also characterized by increased tortuosity of dermal capillary loops which precedes the development of epidermal hyperplasia. Mitotic activity in the basal and suprabasal cells are greatly increased [Dr. George Jacob, Seminar on Psoriasis, Dubai, January 2001]. Cellular invasion takes place, particularly in the suprapapillary region to form the Munro ‘micro abscess’ which are extruded in the horny layer or they may collect in disintegrated malphigian cells, the cytoplasm of which had been lysed to form the multilocular or stratum granulosum of Kogoj.
Stratum granulosums of Kogoj are multilocular pustules in the upper stratum malpighii within a sponge-like network made up of flattened keratinocytes [M. S. Stone and T. L. Ray, DermPath Tutor, Department of Dermatology, Iowa College of Medicine, September 19951. They are seen in psoriasis, Reiter's disease, geographic tongue and rarely in candidiasis. Histological studies, including immunocytochemistry, routine histology and electron microscopy have clearly established that alterations in the blood vessel formation of the skin discussed above are a prominent feature of psoriasis and there is a marked increase in cutaneous blood active edge of the psoriatic plaque [Braverman I M, Yen A. Ultrastructure of the capillary loops in the dermal papillae of psoriasis. J Invest Dermatol 1977: 68: 53-60].
Numerous therapies in the field of allopathy medicine have been researched and developed to reduce dermal vessel tortuosity, to reduce spongiform pustules, and to reduce stratum granulosum disorder, especially in relation to psoriasis.                Treatment of psoriasis-Part I-Topical Therapy and Phototherapy, Mark Lebwohl, MD, et all American Academy of Dermatology, October 2001 Vol 45 (4).        Treatment of psoriasis-Part 2-Systemic Therapies, Mark Lebwohl, MD, et al, American Academy of Dermatology, November 2001 Vol 45(5).        The immunological basis for the treatment of psoriasis with new biological agents. James. G. krueger, M.D, American Academy of Dermatology, June 2002 Vol 46(1) Pages 1-26.        New psoriasis treatments based upon a deeper understanding of the pathogenesis of psoriasis vulgaris and psoriatic arthritis. Jeffrey. P. Callen et al, American Academy of Dermatology, August 2003 Vol 49(5) Pages 351-356.        
However, most of these therapies provide only temporary symptomatic relief and are either unsatisfactory or very expensive and are associated with either short term or long term undesired side effect profiles. [National Psoriasis Conference, Boston Plaza Hotel, Aug. 5-8, 2005, Boston, Mass., USA.]
It is well-known that herbal formulations often have fewer undesirable side effect profiles and hence provide a viable alternative therapy to manage the chronic inflammatory skin conditions that exhibit dermal vessel tortuosity. Research efforts to develop herbal formulations to treat these conditions have been on the rise and there is a continuing need to develop herbal formulations to treat dermal vessel tortuosity, spongiform pustules, and stratum granulosum in keratinization disorders with minimal or no side effects.                Chopra, R. N., Nayar, S. C., and Chopra I. C., Glossary of Indian Medicinal Plants, C.S. I. R., P. 259, 1956.        Murugesa Mudaliar, K. S., Gunapadam (Material Medica) Vegetable Section, Govt. of TamilNadu, P. 527 (1969).        Venkatarajan, S., Sarabendra Vaithiya Muraigal, P. 160, 161 & 167 (1965).        Wealth of India, Raw Materials, Vol. X, P. 588-590, CSIR., New Delhi (1976).        Yugimuni Vaidya Chintamani (800) Stanza 494-51 8, 6. Rathina Nayakar & Sons, Madras, India.        Nair, C. P. R., Kurup, P. B., Pillai, K. G. B., Geetha, A., and Ramiah, N., Effect of Nimbidin in Psoriasis, Indian Medical Journal, October 1978.        